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cardiology first year drugs > cardio drugs > Flashcards

cardio drugs Flashcards

1
Q

moA of ivabradine

A

selective blocker of HCN channels, reduces the slope of pacemaker potential - slow HR reduces oxygen consumption

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2
Q

what is ivabradine used to treat

A

angina, tachycardia, mild to moderate chronic heart failure

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3
Q

side effects of ivabradine

A

arrhythmias and hypotension

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4
Q

what are dobutamine, adrenaline and Noradrenaline

A

b - adrenoceptor agonists

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5
Q

moA of b - adrenoceptor agonists

A

results in stimulation of adenylyl cyclase and production of cAMP which generates protein kinase A. Phosphorylation increases Ca influx and release of Ca from sacroplasmic reticulum increase contractility, force and rate and decrease cardiac efficiency

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6
Q

when are beta adrenoceptors used

A

in infarction, cariogenic shock, cardiomyopathy, inotropic support, heart failure (dobutamine), asthma emergency (adrenaline), anaphylactic shock

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7
Q

SE of beta adrenoceptors

A

arrhythmias and acute MI

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8
Q

what is dobutamine

A

selective for B 1

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9
Q

b1 selective b blockers

A

metoprolol, atenolol

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10
Q

what are propanolol, metoprolol, atenolol

A

beta blockers

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11
Q

MoA of beta blockers

A

decrease HR, contractility, MAP and O2 consumption

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12
Q

when are beta blockers used

A

angina, hypertension, heart failure, thyrotoxicosis

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13
Q

SE of beta blockers

A

asthma, fatigue, cold peripheries, HF - in patients with cardiac failure who rely on sympathetic drive to maintain CO, bradycardia and hypoglycaemia

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14
Q

what is atropine

A

a muscularinic antagonist

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15
Q

what does atropine do

A

it is non selective for M2 receptors and increases HR

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16
Q

when to use atropine

A

reverse bradycardia following MI, adjunct to anaesthesia, anti cholinesterase poisoning (reduces parasympathetic)

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17
Q

SE of atropine

A

arrhythmias, hallucinations, confusion

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18
Q

what is digoxin

A

a cardiac glycoside

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19
Q

Moa of digoxin

A

competes with K at alpha submit and blocks the Na/K pump

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20
Q

what does digoxin cause

A

increased contractility bu blocking the sarcolemma ATPase, indirectly increases vagal activity slowing SA node discharge and directly shortens action potential and refractory period increasing force, contraction and CO - effects are dangerously enhanced with hypokalaemia

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21
Q

when to use digoxin

A

HF, AF

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22
Q

SE of digoxin

A

Heart block, dysrhythmias, myocarditis

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23
Q

what is levosimendan

A

calcium sensitizer

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24
Q

moA of levosimendan

A

binds to troponin C in myocytes sensitising them to Ca

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25
when to use levosimendan
acutely decompensated congestive heart failure and increased contractility
26
SE of levosimendan
headaches, arrhythmias and hypokalaemia
27
what is flecainide
a class I antiarrhythmic
28
what does a class 1 antiarrhythmic do
acts on voltage gated Na channels reducing Na channel current
29
when is flecainide used
for rhythmic control
30
SE of flecainide
negative inotropic effects
31
what are beta adrenoceptors
class II antiarrythmics
32
examples of beta adrenoceptors
propanalol
33
what are class II antiarryhtmics used for
rate control
34
what is amiodorane and sotalol
class III antiarhymic
35
MoA of class iii antiarryhtmics
voltage gated K channels
36
what do class iii anti arrhythmics do
lead to action potential prolongation
37
when are class iii anti arrhythmics used
for rhythm control
38
class IV drug example
verapamil
39
Moa of verapamil
calcium channel blocker
40
what is verapamil used for
rate control
41
what are isorbide mononitrate and GTN spray
nitrates
42
what do nitrates do
mimic the effect of the endothelium, produce nitric oxide which is formed through influx of Ca activation of eNOS and L -argine and NO caused efflux of Ca producing hyper polarisation and relaxation, Endothelin is also produced
43
what do nitrates cause
venorelaxation (decreased preload and after load, CO maintained as HR increases arteriolar dilation and increased coronary blood flow
44
when to use nitrates
in angina and acute heart failure
45
side effects of nitrates
headache, hypotension, tolerance is common
46
what is lisinopril
an ACEi
47
moA of ace inhibitor
block the conversion of angiotensin I to angiotensin II so aldosterone and ADH are not stimulated
48
when to use acei
hypertension and HF
49
SE of acei
dry cough, renal dysfunction ( bad with renal artery stenosis and good for diabetic neuphropathy), angionerurotic oedema, petal abnormalitys
50
what do acei cause
vasodilation and arterial dilatation
51
what is losartan
a ARB
52
Moa of ARB
blocks angiotensin II receptors
53
when are ARB used
hypertension and HF
54
side effects of ARB
renal dysfunction, oedema, no cough, contraindicated in pregnancy
55
what are amlodipine, verapamil and dltiazem
calcium antagonists
56
what do calcium antagonists do
decrease conduction at SA and AV node and cause decrease in HR
57
when are calcium antagonists used
in hypertension, angina and supra ventricular arrhythmias
58
se of CCB
ankle oedema and bradycardia
59
what is doxazosin
an alpha blocker
60
Moa of doxazosin
block a adrenoceptors to case vasodilation
61
when does doxazosin be used
hypertension and prostatic hypertrophy
62
se of alpha blockers
postural hypotension
63
what are minoxidil and nicroandil
k channel openers
64
Moa of k channel openers
hyperpolarisation which switches off calcium channels, mediated by ATP and relaxation of vascular smooth muscle
65
what are k channels openers used for
severe hypertension, angina
66
se of k channels
tachycardia and salt and water retention
67
what is bendrofluazide
thiazide diuretic
68
Moa of thiazide diuretics
inhibit NaCL reabsorption in distal tubules by blocking NaCl co transporter
69
when to use thiazide diuretics
hypertension
70
se of diuretics
hypokalaemia, arrhythmias and fatigue
71
what is furosemide
a loop diuretic
72
Moa of loop diuretics
inhibit NaCl reabsorption in the thick ascending limb of loop of Henle
73
what do diuretics cause
increase in Na, Cl and water and blood volume
74
when to use furesmide
heart failure
75
what are simvastin and atorvastatin
statins
76
what is simvastatin
anticholesterol
77
Moa of statins
blocks HMG- COA reductase which inhibits the formation of cholesterol and lower LDL and total cholesterol inflammation and stabilised atherosclerotic plaque decreases thrombosis
78
when are statins used
hypercholesterolemia
79
se of statins
used in caution with hypothyroidism and history of liver disease - causes myalgia, myopathy, myositis
80
what are bezafibrate and gemfibrozil
fibrates
81
Moa of fibates
agonist of nuclear receptors which enhance transcription of LPL which hydrolysis triglycerides to fatty acids and glycerol
82
when to use vibrates
in high triglyceride levels
83
se of fibres
myositis
84
what are colestyramine, colestipol and colesevelam
bile acid binding resins
85
what do bile acid binding resins do
inhibit cholesterol absorption but casing the excretion of bile salts resulting in more cholesterol to be converted to bile salts it binds bile to the intestine so its not absorbed in the duodenum and uses liver metabolism to cholesterol to compensate for it lost
86
when ti use bile acid binding resins
to cause decreased absorption of triglycerides and increases LDL repepctor expression
87
what do bile acid binding resins cause
GI tract irritation
88
Moa of ezetimibe
inhibits transport proteins and reduces the absorption of cholesterol
89
what does exetimide do
decreases LDL
90
se of ezetimibe
diarrhoea, abdominal pian, headache contraindicated in breastfeeding
91
what is warfarin
anticoagulant
92
how should warfarin be administered
IV
93
Moa of warfarin
blocks clotting factors 2,7, 9, 10 serine proteases glycoproteins precursors of active throbbing factors g carboxylase enzyme is stimulated by bit K and motifs the serine proteases anticoagilants act as fit K antagonists which prevents the production of mature factors
94
when to use warfarin
DVT, PE, NSTEMI, AF
95
Moa of heparin
binds to antithrombin iii increasing its affinity for serine proteases o greatly increase their rate of inactivation
96
what does factor Xa do
activates thrombin IIa
97
what does thrombin IIa d o
causes fibrin
98
what does fibrin cause
blood clot
99
what are dabigatran etexilate and rivaroxaban
orally active inhibitors
100
what dp dabigatran and etecilate inhibit
thrombin
101
what does rivaraxabn inhibit
factor Xa
102
what are aspirin and clopidogrel
anti platelet
103
moa of anti platelets
prevent new throbosis, blocks COX, inhibits formation of TXA2 which causes crosslinkig of platelets blocks ADP from binding to P2Y12 recpetorand formation of fibrin
104
when to use antiplatelets
angina, acute MI, cerebral vascular incident and TIA
105
se of antiplatets
haemorrhage anywhere, peptic ulcer and aspirin sensitivity in asthma patients
106
what are streptokinase, tissue plasminogen activator , alteplace and duteplace
fibrinolytic drugs
107
Moa of fibrinolytic drugs
fibrinolytic cascade opposes coagulation cascade, activate formation of plasmin to form plasminogen which lysis fibrin into fibrin fragments casing lysis of the cot
108
when to use antifibrinolutics
STEMI, PE AND CVA a nd recogen occlude arteries
109
se of fibrinolytic drugs
haemorrhage risk - controlled by tranexami acid which inhibits plasminogen activation

cardiology first year drugs (1 decks)

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